Let me start this blog by saying that I simply don’t know the answers when it comes to the complicated interactions between hard training and thyroid function. And if anyone does, they haven’t published it in the peer-reviewed literature. The spur for this blog entry is an e-mail I got from a friend yesterday with a link to some fitness blog claiming that endurance exercise causes your thyroid to fail and makes you fat. There’s not much point spending a lot of energy debunking every half-baked pseudoscientific theory floating around on fitness blogs – but thyroid function is an interesting one, because the topic surfaces a lot in rumors about elite runners.

Let’s start with a few examples. In about two minutes of Google searching, I found trustworthy references to diagnosed thyroid problems in Alberto Salazar, Adam Goucher, Galen Rupp, Paula Radcliffe, Ryan Hall, and Bob Kennedy. If you read running message boards these days, you’ll find lots of innuendo about Salazar’s runners being diagnosed with “subclinical” hypothyroidism and getting thyroid meds as a result – which, the insinuations suggest, are performing-enhancing through some unspecified mechanism. The first thing to point out is that, while Salazar’s runners are currently in the spotlight because they just won Olympic medals, this doesn’t seem to be some new phenomenon. Salazar’s own diagnosis is mentioned back in a 1987 New York Times article; neither Radcliffe nor Hall nor Kennedy is associated with Salazar (and Radcliffe’s problem was apparently an OVERactive thyroid, rather than an underactive one). Heck, I found an article quoting the coach I’m currently training with, Australia’s Dick Telford, mentioning two of his athletes in the 1990s having thyroid problems. (It also mentions that he himself tested Salazar’s thyroid status – I’ll have to ask him about that!)

But the picture is actually quite a bit more complicated than that. Let’s take a look at the 11 studies that the author cites:

In the first study, the exercise is actually a mix of weight lifting, rowing and running. In a 20-week intense training study, T3 levels initially decreased (as you’d expect with the introduction of a new stress), but by the end of the 20 weeks had returned to initial baseline values – a complete contradiction of the claim that sustained exercise “shuts down production” of T3.

In the second study he cites, it’s once again apparent that he either didn’t read the whole study or didn’t understand it. It involved a group of women running an average of 14 miles per week, who first increased their weekly mileage to 44 miles and then to 64 miles – quite a big jump. Sure enough, the initial jump resulted in a transient decrease in thyroid function... but by the time the runners were at 64 miles per week, their function had normalized again. Though it’s clear that this volume of training is stressful, the authors write, “the absence of a low T3 indicates that this type of stress may differ from other non-thyroidal conditions in its effects on the thyroid axis.”

The third study he cites looked at beginning and experienced rowers across six months of competition, and found no change in T3 levels.

The fourth study involved a group of identical twins who undertook a 93-day training program – and weren’t allowed to eat any more than they did when they were sedentary. Needless to say, this was very stressful on their bodies and caused a broad spectrum of changes, including an average weight loss of 8 pounds and decrease of T3.

The fifth study was actually looking at T3 kinetics – how quickly it’s metabolized, rather than baseline rates – comparing endurance-trained men to controls. The endurance-trained men had the same levels of T3 as the sedentary controls (marginally higher, actually); when they were fed an oral dose of T3, they metabolized it more quickly.

The sixth and seventh studies compared the effects of caloric restriction and exercise on T3 function in women, and found that exercise itself (both quantity and intensity) had no effect of T3 levels. Instead, T3 changes were entirely explained by caloric deficits. In other words, training can lower T3 levels if you don’t eat enough to replace the calories you’re losing.

The eighth and ninth studies were in rats. The tenth study looked at military cadets on a five-day “ranger training course with heavy physical exercise, calorie deficiency and deprivation of sleep.” If this sounds like your training regimen, then I agree that you might have something worry about!

The final study looked at Finnish runners and joggers in the autumn (during “light training”) and in the spring (during “heavy training”). They found that T3 levels were “slightly lower” in the runners during light training but not during heavy training.

Okay, okay, I’m done. The reason I went through these 11 studies so exhaustively is because this is such a prime example of someone making a totally unambiguous claim (“studies demonstrate beyond a doubt...”), citing a pile of studies, and then apparently assuming that no one will actually look at the studies. In this case, I don’t know if it’s deliberate misdirection, or if the guy simply didn’t have access to the full text of the studies he’s citing, or just couldn’t be bothered to read them – but the result is the same.

Now, by no means am I concluding that intense endurance training has no effect on thyroid function! As I said at the top, I don’t know the answers – and I don’t think we should be leaping to conclusions. And of course, this doesn’t say anything about whether thyroid meds could be performance-enhancing. It’s well understood that thyroid function has important roles in (among other things) the regulation of metabolism, cardiac gene function, and bone development. But that’s not the same as showing that it’s actually performance-enhancing. The way I see it, there are a number of possible scenarios:

(1) Endurance training really does shut down your thyroid, and all runners, cyclists, triathletes, etc. are doomed to be fat. I’m comfortable ruling this one out.

(2) Very extreme training over long periods of time down-regulates your thyroid (if you’re susceptible: the twin study cited above suggests there’s a genetic component to response), which is why athletes like Radcliffe, Goucher, Salazar, etc. have been afflicted. To me this is plausible, and remains an open question.

(3) If your thyroid function is low, taking thyroid medication to “normalize” can help you run faster. Again, this is plausible but not (to me) confirmed – and of course, it opens up a difficult discussion about what really constitutes “deficiency” and to what extent supplementation should be allowed.

(4) Thyroid medication is performance-enhancing even if your thyroid is functioning normally, and the diagnosis of problems in elite athletes is just a smokescreen. To me, this seems extremely unlikely, as proper thyroid function is a delicate balance between too much and too little. That being said, “normal” covers a fairly broad range, and there may be room for optimization within that range.

The conclusion? I guess there isn’t really much of one, other than the usual stuff about “more research” and “further questions to be answered.” If anyone has suggestions for other research on this topic I should check out, please let me know in the comments section.

P.S. Okay, one final point in response to that blogger claiming that endurance exercise shuts down your thyroid. There was a study published last year in the journal Hormones, from the University of North Carolina, that compared the acute effects of high-intensity interval training to steady-state endurance training. The findings: 12 hours later, the T3 levels in the interval group were lower than in the steady-state or control groups.